The increase in leg and forearm blood flow induced by insulin could be seco
ndary to its metabolic effect on glucose uptake. We therefore investigated
whether insulin causes vasodilation of the internal carotid artery, since t
he brain is not dependent on insulin for glucose uptake, to demonstrate tha
t the vasodilatory effect of insulin is primary and independent of its meta
bolic effect. Internal carotid artery diameter was continuously monitored u
sing a 7.5-MHz transducer linked to an Acuson XP10 ultrasonograph (Mountain
view, CA) during infusion of 125 mt 10% dextrose mixed with 3 U regular ins
ulin and 5 mmol potassium chloride over 1 hour. The internal carotid artery
diameter increased progressively with time from a mean ol: 5.4 +/- 1 mm to
5.7 +/- 1 mm at 15 minutes, 5.9 +/- 1.1 mm at 30 minutes, 6 +/- 1.1 mm at
45 minutes, and 6.1 +/- 1.1 mm at 60 minutes (P < .05), an increase of 13%
over baseline. Glucose was maintained between 93 and 106 mg/dL, and insulin
increased from 15 +/- 14 mu U/mL and was maintained between 34 and 47 mu U
/mL. There was no change in mean arterial blood pressure (MABP) or heart ra
te during the infusion. We conclude that insulin dilates the internal carot
id artery consistently at physiological concentrations, probably independen
tly of glucose uptake by the brain. Alterations in this effect of insulin m
ay be of relevance in the pathogenesis of abnormalities of cerebral blood f
low in type 1 and type 2 diabetics as described by our group previously. Co
pyright (C) 1999 by W.B. Saunders Company.